56. Attention Deficit-Hyperactivity Disorder

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302 Atten t ion Def ic i t -Hyperac t iv i ty Disorderintel l igence tes ts or nonverbal ada ptat ions of tes ts a re approp r ia te for young er chi ldren w ith aut ismand those w ho have l imi ted ve rba l sk il ls . For ind iv idua ls wi th au t i sm w ho do no t hav e menta l r e ta r-dation, there is a comm on pa tte rn of cogn i t ive st rengths an d w eakne sses , in w hich visual perceptualski lls of ten are s ignif icant ly bet ter tha n v erbal abi l it ies, an d co ncrete problem solving is bet ter thanabstract knowledge. Thu s , in high- fun ct ioning individuals with aut ism, th ere of ten is a learning dis-abili ty profile, which necessitates individual ap pro ach es to edu catio n.

BIBLIOGRAPHYI . Attwood T: Aspergers Syndrome: A Guide for Parents and Professionals. London, Jessica Kingsley2. Bailey A, Phillips W, Rutter M: Autism: Toward an integration of clinical, genetic, neuropsychological,and3 . Bryson S, Smith I: Epidem iology of autism: Prevalence , associated characteristics, and implications for re-4. Cohe n DJ, Volkmar FR (eds): Handbook of Autism and P ervasive Developm ental Disorders, 2nd ed. New5 . Cook EH: Genetics of au tism. Ment Retard Dev Disabil Res Rev : 13-120, 1998.6 Courchesne E: Brainstem, cerebellar, and limbic neuroanatomical abnormalities in autism. Curr Opin7. Dawson G (ed): Autism: Nature, D iagnosis, and T reatment. New York, Guilford Press, 1989.8. Dawson G Osterling J : Early intervention in autism. In Guralnick MJ (ed ): The Effectiveness of Early9. Hagerman RJ, Cronister A (eds): Fragile X Syndrome: Diagnosis, Treatment, and Research. 2nd ed.

Publishers, 1998.neurobiological perspec tives. J Child Psycho1 Psychiatry 37:89-126, 1996.search and serv ice delivery. Ment Retard Dev Disabil Res Rev 4:97-103, 1998.York, John Wiley Sons, 1997.Neurobiol 7:269-278, 1997.

Intervention. Baltimore, Paul H. Brooke s, 1997, pp 307-326.Baltimore, Johns Ho pkins University Press, 1996.

10. Lindberg B: Understanding Retts Syndrom e. Toronto, Hogrefe and Huber, 1991.I I . Lord C, Rutter M, LeCouteur A: Autism Diagnostic Interview-Revised: A revised version of a diagnos ticinterview for caregivers of individuals with possible pervasive developmental disorders. J Autism DevDisord 24:659-685, 1994.12. Lord C, Rutter M , Di Lavore PC: Au tism Diagnostic Observation Schedule-Generic. Chicago , Universityof Chicago Department of Psychiatry, 1998.13. Schopler E, Reichler RJ, Renner BR: The C hildhood Autism Rating Scale (CARS). Los Angeles, WesternPsychological Services, 19 88.

56. ATTENTION DEFICIT-HYPERACTIVITYDISORDER

William W. D o d s o ~ , . D

1. What is attention deficit-hyperactivity disorder ADHD)?Th e f ir s t descr ipt ion s of ADHD appea red a t the turn of the century, and the cur ren t med icat ion

treatment w as f i rs t descr ibed in 1937. Ou r unde r st a nd ing of the d i sorder has deve loped ov er t ime ,and the n ame and d iagnos t ic c r i te r ia for ADHD have changed wi th tha t under s tanding . Th e cur r en tdiagno sis as i t i s descr ibed in the DSM-IV is: I ) a pers is tent pat tern of inat te nt iod easy dis tractibi l-ity, (2) behavioral an d emo tional impuls ivity, and sometimes (3) hyperactivity o r severe restlessness.Th ese sym ptom s are s ignif icant ly m ore severe than is typical in pe rsons of a s imi la r deve lopmenta lleve l . I na t ten t ion , impuls iv i ty , and r es t l e s sness mu s t cau se s ign i fican t impa i rme nt in a t l eas t twoareas of funct ion ( school , peer re la t ionships , family re la t ionships , and work, mo od regulat ion, an dse l f -es teem) and m us t have been cont inuo us ly presen t for a t l eas t 6 mon ths . For examp le , a ch ildw ho m i s be ha ve s i n t he c l a s s room a nd i s d i s r up ti ve , bu t do e s no t e xh i b i t s i m i l a r p r ob l e m s o n t hep layground or a t home, does no t mee t d iagnos t ic c r it e ria .


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Attention Defici t-Hyperact ivi ty Disorder 303DSM -IV Criteria f o r Attention DeJicit-Hypeructivity Disorder

InattentionSix or more of the following, manifested ofteften:Inattention to details/makes careless mistakes

Difficulty sustaining attentionSeems not to listenLose s things ForgetfulFails to finish tasksImpulsivity/Hyperactivity

Difficulty organizingAvoids tasks requiring sustained attentionEasily distracted

Six or more of the following, man ifested oftenBlurts out answer before question is finishedDif iculty awaiting turn

Impulsivity HyperactivityFidgetsUnable to stay seatedInappropriate running/climbingAlways on the goRestlessnessDifficulty in engaging in leisure activitiesquietlyTalks excessivelyInterrupts or intrudes on others

The symptoms of inattention or impulsivityhyperactivity:have persisted for 6 months or longerare more frequent and s evere than is typical of the individuals level of developmenthave onset prior to age 7cause so me impairment in two or more s ettings (i.e., cause significant impairment in social.are not better accounted for by another men tal disorderacademic, or occupational functioning)

2. What are the behavioral signs of ADHD?Th e presentat ion of AD HD varies depending on the a ge and developm ental level of the pat ient .Preschool Ages 3-5)Always on the goAggressive (hi ts or pushes others)Dangerously daringNoisy, interrup tsExcessive temper tantrumsInsatiable curiosityLow levels of complianceAdolescent Ages 13-18)Restless, rather than hyperactiveSchoo l work disorganized andProcrastination on mo st tasksEngages in risky behavior (speeding,Poor p eer relat ionshipsPoor self-esteemDifficulty with auth ority figures

incomplete

drug experimentat ion)

Elementary School-Age Ages 6-12)Easily distracted, hard to stay on taskHom ework poorly organized, incomplete,

and contains careless errorsImpatient, blurts out answ ers, fails to waitturn in gamesOften out of seatPerceived as immatureAdulthoodDisorg anized, fails to plan aheadForgetful, loses thingsMult iple jobs, relationshipsMisju dges tim e available, freq uently lateMo od labili ty and flash anger outburstsMany projects started but few com pleted

3. s hyperactivity required for the diagnosis?No. Wh ile the hyperac t ive fea tures a re unmistakable w hen present (and, therefore , were themain focu s of ear l ie r d iagnost ic f ramew orks) , w e now know tha t fewer than ha l f of persons w i th


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304 Attention Deficit-Hyperactivity DisorderADH D are hyperactive. True hyperactivity is much more com mon in boys, leading them to be iden-tified and treated much more frequently than girls. When hyperactivity is absent, the individuals stillare restless, talk incessantly, commonly lose the point of what they are saying, fidget, may be out oftheir seats walking around, pat their feet or fingers tirelessly, and/or cannot turn off their minds tofall asleep at night.

4. What causes ADHD?The exact cause remains unknown, but there usually is a clear genetic clustering of cases in fam-ilies. Adoption stu dies identify that genetics are far m ore im portant than environment in the manifes-tation of the disorder. Twin studies do not show com plete concordance , indicating that other factorscontribute to the etiology of ADH D. However, to date the only facto r clearly demonstrated to belinked to the disorder is maternal sm oking during pregnancy. Six studies of twins with ADHD showconcordance rates of 60-80 .5. Does ADH D persist into adulthood?In the time when diagnostic schemes heavily focused on hyperactivity, it was believed thatADHD was a lag in developmental maturation that would go away with age. In the years that fol-lowed, however, as the genetic basis was identified and as children w ith AD HD grew up to be adultswith continuing sym ptoms and impairment, it was recognized that adults can have ADH D. Ther estill are no form al DSM criteria for adu lts, wh o must be given the diagnosis of ADHD-In PartialRemission or Not O therwise Specified.The rate of persistence depends on how persistence is defined. If using the strictest definitionof being diagnosed as a child and con tinuing to meet full criteria as an adult, the persistence rate isabout 33 . If persistence is defined as probably having m et criteria in childhood and currentlymeeting 5 out of 9 criteria (instead of 6 out of 9), the persistence rate jum ps above 80 . Luckily,

adults continue to respond to the sam e medications and interventions as children do.Often, people diagnosed as adults have additional therapy to d o as they m ourn all of the timeand opportunities lost due to not being treated fo r their condition. They m ust also rework a sense ofwho they are as people w ith ADH D: they are not lazy, stupid, or crazy.5a6. How common is ADHD?ADH D is the most com mon behavioral condition diagn osed in children. The DSM -IV reports aprevalence in children of 3-5 . Wh en studies were done, however, to determine the imp act onprevalence rates of the DSM-IVs emphasis on inattention, researchers were surprised to discovermuch higher rates both in Tennessee, where every child of school age in an entire county was

screened, and in Germ any, where the identical study had been performed a year earlier. Both studiesdemonstrated rates in excess of 10 .Based on new criteria, studies have shown prevalence rates for purely inattentive individuals(4.9-9 ) in addition to the impulsivehyperkinetic (3.4-3.9 ) and combined subtypes ( 4 . 4 4 8 ) .More girls are identified using the DSM-IV criteria than ever before.7. Is ADHD over-diagnosed and over-treated?This perception has arisen from a number of factors:Increased awareness of the condition by the publicAcceptance of a broader set of diagnostic criteria

Greater appreciation of the cou rse of the illness and its ultimate impact on adult life, whichjustifies lengthier and uninterrupted treatmentsDiminished concern about growth retardation, predisposition to drug use, and long-term ef-fects of stimulant class medicationsIncreased treatment of adults.In fact, the condition still goes unrecognized and untreated most of the time. Even assuming thelower end of the traditional prevalence estimates (3 ), fewer than one in three affected children everget diagnosed and treated.


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Attention Deficit-Hyperactivity Disorder 3058. How is ADHD diagnosed?The diagnosis of ADHD is a clinical diagnosis derived from a careful history taken from manyindividuals and sources. The more data available to the clinician, the better. The process begins bytaking a history-either from the childs parents or from the adult patient directly-of persistent,lifelong behavioral patterns that cause significant impairment in every area of the patients life.Various researchers have assembled the common symptoms of ADHD into scales and checklists.Among the best available are:

AD HD Rating ScalesFor Clinicians: For Teachers: For Parents:Brown scales Connors Teachers List Conners Parents ChecklistAuchenbach scale Vanderbilt Teachers Rating ScaleADHD ComprehensiveTeacherRating Scales (ACTeRS)

School records and report cards are helpful to establish longitudinal patterns of distractibility, behav-ior problems, and failure to perform up to potential.9. W hat is the differential diagnosis of ADHD ?A careful history must be taken to rule out conditions that may be mistaken for ADHD. This iscomplicated by the fact that ADHD may coexist with any of these conditions.

Dtffei-entialDiagnosis o AD H DCoexisting ConditionsConduct disorderOppositional defiant disorderLearning disabilitiesAnxiety disorderMood disorderSpeechnanguage disorder

Possible Etiologic ConditionsChronic lead poisoningPost-traumatic or infectiousEncephalopathyFetal alcohol syndromeFragile X syndromePhenyl ketonuria

Differential ConditionsAge-appropriate high activityMental retardationThyroid disordersAbsence seizuresSensory deficitsTourettes syndromeTic disorderSleep disordersAspergers or autismPsychosisSubstance abuseEnvironmental ConditionsAbuse or neglectFamily adversitySituational stressHigh intelligence with inappropriateschool placement

10. Wh ich laboratory tests are helpful?None. Sometimes standard IQ test subtests that involve attention (e.g., Digit span) draw scoresthat are significantly lower than other subtest scores, or there may be subtest scatter in which thesubtest scores vary by more than 4 points. IQ testing scores may be available due to previous acade-mic failure, but should not be obtained as part of an ADHD assessment unless comorbid specificlearning disorders also are suspected. Computer-based continuous performance tests (e.g., the TOVA[Test of the Variables of Attention] or Conners test), which measure attention span and impulse con-trol directly, are available. These tests cannot be used to make or deny the diagnosis since they havemany false-negative tests and measure inattention/irnpulsivity from any etiology, not just ADHD.Their utility lies in research and in objective determination of the optimal dose of medication. EEG


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306 Attention Deficit-Hyperactivity Disorderrhythm analysis an d various scans (e.g., SPECT, PET ) currently are being studied, but have not yetdemonstrated sufficient validity to justify their high cost. They are not considered a part of the eval-uation of ADH D except in the most complicated cases.Once m edication therapy has begun, b lood levels of stimu lant class medications are not useful,since there is no correlation between blood level and effect upon the sym ptom s of ADH D.11. Discuss the controversies surrounding the diagno sis of ADHD.The diagnosis often is difficult to make for a number of reasons:No specific diagnostic test is available.The symptoms are nonspecific and can be found in a number of medical and psychiatric con-ditions.The core s ymp tom of inattention is invisible. (Only the patient is aware that his or her attentionhas wandered. Learned social behaviors m ask the fact that the person is no longer paying at-tention.)There often is a low rate of agreement between different informants (patient, teachers, parents,and spou ses).Many people d o not mak e a clear distinction between having an explanation and having anexcuse for misbehavior and failure. It is a cornerstone of American values that any problemcan be overcome if you buckle down, work hard enough, and have sufficient self discipline.The reality that som e people are born hardwired to be inattentive, impulsive, and fidgety goesagainst this tenet of faith.The best treatment for ADHD is the stimulant-class medications. These schedule C-I1 drugsmake many physicians an d parents uncom fortable and are inconvenient to prescribe; henc ethere is reluctance to diagn ose.The diagnosis, treatment planning, and patien upa rent education are time consuming and do

not fit well into the busy schedules of physicians, parents, and teachers.12. What is the impact of ADHD on patients lives and the consequences of not treating th econdition?Almost without exception, every study of the impact of ADHD on people with the condition hasshown compelling evidence that ADHD has a detrimental effect upon the ind ividuals life. Tw enty-fivepercent of affected individuals m ust repeat at least one grade in spite of adequate academ ic ability.Despite similar IQ scores and educational attainment, individuals with untreated ADHD have lower oc-cupational attainment and job satisfaction. Adolescents with ADH D who do not take m edication havebeen show n in three studies to be four times more likely to have injury-producing accidents than ado-lescents with AD HD who d o take m edication. An old jok e that ADD actually stands for AccidentalDeath and D ismemberment illustrates the strong connection between ADH D and traumatic injury.Adolescents with A DH D have m uch higher risk fo r self-inflicted injuries than d o adolescentswithout ADHD I3 vs. 0.1%).By the age of 27 the rate of subs tance use disorde rs in person s with ADH D w ho do not takemedication is 300 higher than the general population (47 vs. 15 ). Patients who continue totake stimulant-class medication for their ADHD have the sam e risk of d eveloping substance use dis-orders as does the general population. Stimulant-class medication is protective against the develop-ment of these disorders in adolescents and young adults with ADH D.It is becoming mo re clear as time goes on that the risk lies in not treating A D H D rather than inusing stimulant-class medications.13. What constitutes optimal treatment for ADHD ?The current gold-standard treatment for AD HD i s stimulant-class medications. There are nowover 170 controlled studies demon strating that these m edications are most effective, as well as safe.Additionally, they continue to be effective without the development of tolerance. It is this latterfactor that leads many researchers to look for a mech anism of action other than their stimulant prop-erties. For now, we must say that their mode of action fo r persons w ith AD HD is unknown.


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Attention Deficit-Hyperactivity Disorder 30714. Elaborate on the stimu lant-class medications.Stimulants have been used to treat ADHD for a long time. Since Bradleys original article in1937, we have had more than 60 years of experience with amphetamine and 30 years of experiencewith methylphenidate, with no negative effects identified from chronic administration.There are three commonly prescribed stimulant-class medications. They come in various imme-diate and long acting forms:

Generic Name Trade Name DosageMethy lphenidate Ritalin, Methylin 5,10,20 mgRitalin SR 20 mgMetadateer 10,20 mg

Dexedrine SpansuleDextroamphetamine Dexedrine, Dextrostat 5, 10mgd, 1 Amphetamine salts Adderall 5, 10,20, 30 mg

5 10, 1.5 mg

15. Wh ich stimulant is best for ADHD?Methylphenidate (Ritalin) is by far the most commonly prescribed medication for ADHD, butthis pattern is changing as clinicians become familiar with the long-acting preparations of ampheta-mine (Dexedrine Spansule, Adderall). Five recent double-blind studies comparing methylphenidatedirectly to Adderall seem to show that the amphetamine product is superior to methylphenidate intreating the core symptoms of ADHD-but more research is needed.The sustained release (SR) fornwlations of methylphenidate are unreliable and come in only onedosage strength (20 mg), which cannot be cut without losing the sustained release effects. Consequently,the Ritalin SR formulation is not recommended or used by most practitioners.Note that medication alone is rarely enough to treat the many impairments of ADHD ade-quately. Pills dont give skills Medication levels the neurologic playing field so that individuals withADHD can have an equal chance at life and begin to do the remedial work necessary to rebuild theirlives, work, and relationships.

16. How is the optimal dose of medication determined?For many years practitioners used weight-based nomograms to determine the dose of stimu-lant. This was largely a misunderstanding. The nomograms had been taken from the originalblinded studies that demonstrated the effectiveness of this class of medications. The nomogramswere intended to protect the double-blind conditions and were not recommended as the best wayto determine the right dose of medication. We now know that the dose at which a unique individ-ual gets optimal benefit varies widely from as low as 1 mg per dose to as high as 40 mg per dose.There is no known way to predict the optimal dose. It usually is found through a trial-and-errortitration.Take home message: Optimal doses vary widely and must be fine-tuned to each patient. Mostpatients detect a difference in their function even at a dosage change of 2 mg. More is not better. Thedose that achieves optimal focus of attention, impulse control, mood stability, and no side effects isdifferent for each patient17. Describe a trial-and-error titration.

A typical titration protocol starts with just 2.5 mg of medication every 4 hours for methyl-phenidate or immediate release dextroamphetamine, and every 5 to 7 hours for long-acting ampheta-mine products. The dose is then increased by 2.5 mg of medication every 1-3 days. With eachincrease in dose the patient should notice a clear improvement in performance, impulse control, andmood stability, without side effects other than mild appetite suppression. At some point, the dose isincreased by 2.5 mg but the patient doesnt notice any improvement over the previous dose. At thatpoint, the optimal dose for that individual is the lower of the two doses. This dose does not changefor many years; tolerance does not develop.


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308 Attention Deficit-Hyperactivity DisorderClinical Pearl: All of the stimulant-class medications are moderately strong bases (pH 12-1 3).If these m edications are present in the lum en of the gut with orga nic acids such as citric acid orascorbic acid (vitamin C), the stimulant medication is ionized and canno t be absorbed from the gutinto the blood stream. The following foods should be avoided for hour before and after taking a

dose of stimulant class medication:Citrus fruitCitrus juicesFruit juices with citric acid as a preservativeSo das hrb on ated beverages

Kool Aid, lemonade, G atoradePoptarts, granola bars, breakfast barsOral suspension medicationsVitamins and food supplements containingvitamin C18. What are the adverse effects of stimulant-class medications?At the dose that is optimal for a given individual, there should be no side effects other than atransient loss of appetite. The ad verse effects that d o occur g enerally are m ild, short lived, and re-sponsive to sm all decreases in do se o r adjustments in the timing of doses.

The more com mo n adverse effects reflect overdosage and include insomn ia, jitteriness, irritabil-ity, headache (especially as a dose wears off), mild hand tremor, and palpitations. Stimulants mayunmask a tic disorder, but do not cause tics. In very rare instances, stimulants can precipitate a psy-chosis. Wh en psychosis o ccurs, a coexisting diagnosis of eithe r bipolar mood disorder or schizo-phrenia m ust be considered.There was once a concern that stimulan ts caused grow th retardation in children. W hen this hasbeen found, compensatory growth alw ays has occurred, and each subject has ultimately reachedtheir full predicted stature.19. Does treatment of ADHD with stimulant-classmedication lead to future drug abuse?

Several prospective studies demon strate that treatment of AD HD w ith first-line stimulant classmedications seems to protect against the development of substance use disorders. The risk comesfrom not treating ADH D.20. Are there other stimulant medications used to treat ADHD?Pemoline (Cylert) is a derivative of methy lphenidate that is effective for about 70 of personswith ADH D. In m ultiple clinical trials, pem oline has been shown to be effective in doses of 75-100mg given once a day in the mo rning. Unlike the other stim ulants which are completely effective assoon as they are absorbed, pemo line often requires 3 weeks to accumulate effectiveness.The major side effect is difficulty falling asleep. Rarely, children develop hepatotoxicity,whichhas been fatal in more than 20 cases w orldwide. Although liver function studies are recomm endedevery 2 4 weeks for at least the first year of treatment, several cases of hepatotoxicity have been soquickly p rogressive that LFTs would no t have caught the hepatitis in time. Due to the potential forfatal hepatotoxicity, the FDA no longer recommends pemoline as a first-line med ication. Nonetheless,it is a good alternative for the patient at risk of substan ce abuse or who is so disorganized and forget-ful that once-a-day dosing is all they can manage.21. Discuss the use of second-line medications.The seco nd-line medications are second for two reasons: (1) they are only abo ut half as effectiveas the first-line stimu lants, and (2) their effectiveness commonly decreases over time and may sud-denly sto p altogether. Since their m echanism of action is unknown, it is not known why this tachy-phylaxis occurs.Th e tricyclic antidepressant (TCA ) medications imipramine and desipramine have been usedlongest. Som e research recommends doses of 2-4 mg/kg, while other literature recommends lowdoses of no m ore than 60 mg/day even for adults. Either way, TCAs slow cardiac condu ction, and anEKG is recomm ended b efore initiation of therapy. TC As m ay be the best choice fo r the patient withmild to moderate ADHD and comorbid depression or panic.Buproprion Wellbutrin) is an antidepressant that has metabolytes similar in clinical structureto amphetamine. T hree studies report that buproprion improved the cor e symptoms at doses up to


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Attention Deficit-Hyperactivity Disorder 309400 mg/day in adults and 150-250 mg/day in children. Buproprion usually is well tolerated, withmild headache, nausea, and insomnia the most com monly reported side effects.One study reports a significant benefit for adults w ith ADHD from v enlafax ine (E ffexo r) at 75mg bid.22. W ha t is the role of a lpha-2 agonists?The two alpha-2 adrenergic agonists currently on the ma rk et 4 lo n id in e (C atapres ) and gua n-fa ci ne (Tenex)-have been extensively studied. Th e hyperactive sym ptom s respo nd best to thealpha agonists, but they have no effect on other core symptoms of inattention and impulsivity.Consequently, the alpha agonists almost always are used in conjunction with stimulant-class med-ications especially in the treatment of children with significant hyperactivity.Th e alpha ago nists have extr a utility for patien ts with co existing tics an d/or Tourettes syn -drom e. Their side effects of sedation also may be useful to help patients w ith AD HD shut off theirbrains and bodies to fall asleep at night.

Treatment is started at low doses (one-half of a 0.1 mg-tablet of clonidine twice a day) and in-creased gradually to allow development of tolerance to the sedative side effects and because the de-crease in hyperactivity m ay take 2 weeks or m ore to develop. Once the optimal dose is determined(0.2-0.4 mg/day of clonidine), it can be administered by a transdermal patch. Alpha ag onist treat-ment should not be discontinued abruptly du e to the potential for hyp ertensive rebound.The com bination of stimulants and clonidine was studied extensively following reports of fivedeaths of children prescribed this combination. The medications seemed to have no causal linkage tothe deaths, and the combination is now considered to be both safe and effective.23. W hat modal it ies are no t effect ive for th e t reatm ent of ADHD?

More than 20 studies have refuted the claims of dietary m anipulations, such as the F eingold dietor elimination diets. Other interventions that have been shown to be largely ineffective in treatingcore symptoms are:Individual psychotherapy Chiropractic manipulationCognitive therapy MegavitaminsPlay therapy Eye movem ent therapyEE G biofeedback Trying harderAllergy treatmentsBIBLIOGRAPHY

I . American Academy of Child and Adolescent Psychiatry: Practice parameters for the assessment and treatmentof attention-deficit hyperactivity disorder. J Am A cad C hild Adolesc Psychiatry 3 6(Su ppl 10):85S-121S,1991.2. Biederman J, Wilens TE, Mick E, et al: Pharmacotherapy of attention deficithyperactivity disorder reducesrisk of substa nce use disorder. Pediatrics 104(2), nternet edition, p e20, 1999.3. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, DC, American PsychiatricAssociation, 1994.4. Elia J Ambrosini PJ, Rapoport JL: Treatment of attention-deficit-hyperactivity disorder. N Engl J Med340:78&788, 1999.5. Goldman LS, Gene1 M, Bezman RJ, et al: Diagnosis and treatment of attention-deficithyperactivity disorderin children and adolescents. JAMA 279: 110 G1 107 , 1998.5a. Kelly K, Ramundo P: You Mean Im Not Lazy, Stupid, or Crazy? New York, Scribner, 1995.6. Pliszka SR: Comorbidity of attention -deficith ypera ctivity disorder: An overview. J Clin Psychiatry 59(Suppl7. Wolraich ML, H annah JN, P innock TY, et al: Comparison of diagnostic criteria for attention-deficit hyperac-8. Zametkin AJ, Ernst M: Problems in the management of attention-deficit-hyperactivity disorder. N Engl J Med9. Zametkin AJ, Liotta W: The neurobiology of attention-deficit/hyperactivity disorder. J Clin Psychiatry

7 :50-58, 1998.tivity disorder in a county-wide sample. J Am Acad Child Adolesc Psychiatry 35:319-324, 1996.340:40116, 1999.59(supp l 7) : 17-23, 1998.

56. Attention Deficit-Hyperactivity Disorder

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